Subjects with Alzheimer's disease (AD) may have low levels of circulating lactate and pyruvate but normal plasma ketone bodies (KBs, b-hydroxybutyrate and acetoacetate). In this paper, we point out the underlying mechanisms for the above findings. Low lactate and pyruvate may be accounted for by abnormalities in glycolytic and aerobic pathways, such as reduced glycogen store and/or decreased levels of glucose transport, decreased phosphofructokinase activity, and increases in oxidatively modified glycolytic enzymes. The fact that patients had normal levels of KBs suggests that they were not starving and that their dietary intakes were normal. There are potentially two negative practical consequences of these metabolic abnormalities: reduced residual physical performance and lower provision of energy substrates to several organs including the heart
Metabolic Mechanisms Underlying Low Circulating Lactate and Pyruvate in Subjects With Alzheimer's Disease
Verri M;Buonocore D;Dossena M
2019-01-01
Abstract
Subjects with Alzheimer's disease (AD) may have low levels of circulating lactate and pyruvate but normal plasma ketone bodies (KBs, b-hydroxybutyrate and acetoacetate). In this paper, we point out the underlying mechanisms for the above findings. Low lactate and pyruvate may be accounted for by abnormalities in glycolytic and aerobic pathways, such as reduced glycogen store and/or decreased levels of glucose transport, decreased phosphofructokinase activity, and increases in oxidatively modified glycolytic enzymes. The fact that patients had normal levels of KBs suggests that they were not starving and that their dietary intakes were normal. There are potentially two negative practical consequences of these metabolic abnormalities: reduced residual physical performance and lower provision of energy substrates to several organs including the heartI documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
